This project focuses on the role of cervical propriospinal neurons in the regulation of sympathetic activity (SA). These neurons mediate spinal sympathoinhibition which resembles previously- described sympathoinhibitory processes of unknown mechanism(s) which are probably important for the organization of sympathetic discharges of appropriate magnitude and duration. We will test the hypothesis that a cervical sympathoinhibitory system is tonically active in animals with intact cords and that it is driven by supraspinal systems. We will determine whether this cervical system normally regulates the distribution and temporal properties of sympathetic discharges. We will also determine the abnormalities in sympathetic regulation which occur when this system is disabled. We will seek the neuroanatomical substrate for the cervical regulation of SA by tracing propriospinal connections between cervical and thoracolumbar cord. We will determine whether these connections are direct or "reticular" in nature. We will determine whether cervical cord plays a role in regulatory processes such as the "sympathetic silent period" and sympathoinhibition elicited by afferent stimulation. The interactions between this propriospinal regulation of SA and supraspinal regulation of SA will be studied at the level of single cervical neurons. We will identify interneurons which are candidates for sympathetic regulation using correlation techniques. Then, we will determine the responses of these neurons to reversible blockade of descending supraspinal influences and to reversible blockade of synaptic transmission of cervical systems. The behavior of these neurons during a variety of centrally- and peripherallyelicited sympathoinhibitions will be studied to determine which of these phenomena are mediated by similar spinal processes. These experiments will improve our understanding of the way in which spinal cord organizes supraspinal, spinal, and afferent information to regulate the intensity, duration, and distribution of SA. This information will provide the basis for understanding the aberrations in sympathetic processing which follow spinal transection.